Behind every vaccine is an assumption. That HPV causes cervical cancer, that
cervical cancer causes death, and that a vaccine can effectively interfere with
this linear relationship is the assumption to be examined in this article.
Cervarix is a vaccine recommended to girls beginning as early as 9 years old,
intended to protect against HPV strains 16 and 18 upon completion of a 3 dose
series. It is an
aluminum-containing product,
with notable "immunogenicity".

A new GlaxoSmithKline (GSK) funded study published in the Journal
of Infectious Diseases has revealed that HPV infection, resulting in
naturally acquired human papilloma virus (HPV) antibodies, reduces the risk for
new infection and cervical abnormalities linked to cancer in non-HPV vaccinated
subjects.

If, in fact, the HPV vaccines do not work as widely advertised, and natural
HPV infectious exposuresactually protect against the progression of HPV linked
cervical changes to cancer, then taken together, both these findings challenge
the most fundamental assumptions within vaccine science (aka vaccinology), and
render highly dubious the oft repeated rhetoric that natural HPV infection is
juggernaut –like deadly force the best defense against which are universal
immunization campaigns.

HPV Infection Protects Against New Infection and Cervical 'Premalignancies'

It should be noted that this is one of the first studies to look at the
natural history of HPV infection and immunity, as well as one of the first
studies to show the validity of using the control arm data from vaccine efficacy
trials. The control arm did, however, receive three doses of the Hepatitis A
vaccine. As there are no vaccine studies in existence using a true
non-vaccinated control group, the natural incidence of a disease, as well as the
true risks of a vaccine cannot be effectively assessed.

The study found that the presence of natural antibodies against HPV16,
considered one of the most malignant of the over 120 unique types
identified, lowered the risk for newly detected infection and a type of abnormal
pap smear result known as ASC-US+ or 'atypical squamous cells of undetermined
significance'. The same protective effect was found for natural HPV18
antibodies, only to a lesser extent.

While the presence of HPV antibodies (seropositivity) overall was not
associated with the development of the so-called cervical 'premalignancy' known
as CIN1+, i.e. cervical intraepithelial neoplasia grade 1 or higher, those with
the highest antibody levels at baseline had a significantly reduced risk of
developing CIN1+ compared to women without detectable HPV antibodies (seronegative
women).

Given that the entire justification for vaccination is based on the
observation that surviving natural exposures to infectious challenges results in
lasting immunity, this finding is not that surprising. HPV is no doubt one of
countless infectious challenges the body's elaborate and highly effective
adaptive immune system countermands, often subclincally/asymptomatically[1] .
Even the authors of the study acknowledged: "Naturally acquired antibodies can
remain detectable for at least 4 to 5 years, albeit at much lower levels than
those induced by vaccination." Given the outcomes demonstrating protective
efficacy of these lower levels of antibodies, questions may be raised about
other elements of the immune system at play in successful pathogenic defense.[2]

The study brings to the fore three major realizations:

Vaccine science is in its infancy, as we are still
elucidating the role of antibodies, natural or synthetically stimulated. As
we discussed in a
previous article under the heading 'Beyond Antibodies,' the
vaccine-inducible increase in antibody titers (often called "efficacy") does
not ensure antibody-antigen affinity, the only likely relevant proxy
measurement of real world vaccine effectiveness; furthermore, the entire
antibody-centered view of vaccine effectiveness has been called into
question by
a recent study, including the following three well-known problems with
the antibody-driven model:

The authors reference the acquisition of identifiable antibodies in only
50-70% of women infected with HPV-16 or 18. What is happening in the rest of the
cases? The authors suggest that those with previous infection but without
antibodies may have mounted a cell-mediated response that also conferred
protection not assessed in this study (or acknowledge to be relevant by vaccine
manufacturers). This is tacit acknowledgement of the biochemical individuality
that underlies immune response, rendering a reductionist one-size-fits-all model
inappropriate for preventive medicine.

2. It appears there is a correlation between antibodies related to infection
and protection from dysplasia (cellular abnormalities) rather than infection
progressing definitively to cancer. The commonly held notion that naturally
transmitted HPV infection and subsequent elevation of antibody titers is a
disease process that leads inevitably to tissue pathology and possibly precancer
or cancer, rather than an instance of the immune system effectively meeting the
HPV viral challenging and responding with an appropriate antibody response,
conferring lasting immunity, is debunked by this new study. Clearly, natural
infection not only prevents reinfection, but even reduces the risk of HPV's
potential induction of dysplastic cellular changes associated with cancer.

3. An acknowledgment of the unknown differences between vaccine-induced and
natural antibody-mediated immunity. The authors of the study noted that there
are "some differences between naturally-acquired versus vaccine-induced antibody
production." They discuss that while vaccine-induced antibody increases are far
higher (as much as 45x higher), "antibody properties such as affinity, avidity,
and specificity may also be different." Remarkably, the study found a
statistically significant quantitative relationship between antibody titers
acquired naturally through "HPV-16 infection and the incidence of newly detected
and 6-month persistent HPV-16 infection and HPV-16 associated ASC-US+,
respectively." They observed a 90% risk reduction of incident infection in
association with antibody titers of approximately 370, 204, and 480 EU/ml. And
yet, the authors emphasized that "these values do not represent correlates of
protection with regard to antibody levels induced by vaccination," since in thePATRICIA
trial vastly higher antibody titers were generated 1 month after the full
vaccination course: 9341, 4769 EU/ml for HPV-16 and HPV18, respectively, but
without exponential increases in vaccine effectiveness, as would be
expected if antibody titers alone were a measure of effectiveness.

Additionally, the authors insinuate that natural HPV infection may be
superior to HPV vaccination by conferring more encompassing protection against
HPV subtypes:

Thus, natural infections are likely not restricted to the generation of L1
antibody responses but would be expected to include a spectrum of HPV-specific
cell-mediated and humoral immune responses that could contribute to reduction in
new infection.

Given the possibility that HPV infection itself confers protection against
HPV reinfection and its more serious health implications (e.g. CIN1+), and that
the HPV vaccine may not offer the same level of protection that our inborn
adaptive immune responses to natural HPV infection does, we should pause to
question the dominant HPV memes circulating out there – via the CDC, the
pediatricians, the mainstream media – that proffer HPV is a
'vaccine-preventable' disease that we are morally and socially obligated to
engage 'preventively' through vaccinating every susceptible adolescent on the
planet. This fear-borne meme driving the herd to vaccinate against HPV—and
everything else —is at least as infectious as the very virus they falsely
promise their bivalent and quadrivalent vaccines will defeat.

When we consider that the HPV vaccine has recently been found to present an "unavoidable"
vaccine danger to those to which it is administered, that the PATRICIA
trial found 35-36% of the subjects had "medically significant" adverse
effects, and that a growing body of peer-reviewed
published literature already links it to over a dozen serious health side
effects including death, what does a sane parent do? There is a growing chasm
between policy makers driving mandatory HPV vaccines into schools, homes and
workplaces, and the voice of reason and the precautionary principle that stands
firm against any obviously unnecessary medical intervention that has not been
adequately proven safe in extensive animal and human clinical trials.

If we are to establish safety and efficacy in the realm of a pharmaceutical
product that is delivered to all individuals without regard for genetics,
pre-existing conditions such as autoimmunity, inflammatory or neuroendocrine
status, it is essential that vaccinated versus unvaccinated (without delivering
adjuvants such as aluminum as a control) long-term trials be undertaken. The
grounds for dismissal of this most basic clinical trial are steeped in
propaganda such as "vaccines are safe and effective, such that withholding them
is an unethical assault on public health". Perhaps it's time for us to truly see
how safe and effective they are by engaging in basic scientific methodology. We
might find that everything we thought was true, is far from it.